NACH, as GGR and kelkel have already stated, the powder ryr from HR is the way to go. I honestly don't see how sup suppliers can sell the pill forms from the US as cholesterol lowering supps when the FDA has regulated the beneficial compound out of it.
Update:
As stated I stopped the RYR maybe 3-4 months prior to blood work I just had done. The goal was to see if I could hold onto the positive changes I made without using it and thus, eliminate it from my protocol. Well my BW came back great! My LDL particle size remained "Pattern A, Large Buoyant LDL" so I'm excited about it. It means I'm holding that level without the use of the natural statins in RYR.
My doc is very happy with this as well. Only time will tell if it holds there until my next BW in six months, but I see no reason why it should not. So far this experiment has validated the use of this protocol, imho. Hopefully it works for someone else as well.
kelkel, did you maintain the niacin and NAC, less the ryr?
Yes, I totally agree. It's a shame you have to request that particle size be monitored. I also take NAC as a daily sup for other benefits as well. I also take Vitamin C with the NAC. I've read that it helps to reduce the oxidation of the NAC. Not sure about the validity of that but I look at Vit C like I do NAC...it's too cheap with too many positives to not incorporate.
Thank you for sharing your experiences and knowledge kelkel!
I don't see it available on Amazon anymore but can buy it from hard rhino dot com. No space between hard and rhino.![]()
When I tried ryr it made me sick as hell! Gave me flu like symptoms, nausea, and body cramps. Do you guys think my body just doesn't work will with it or it was a bunk product?
Hard rhino powder has certificates for theirs which makes me think ryr is under dosed or faked.Originally Posted by GingerbeardJ
How long did it take using the RYR and other stuff to get it down? I use everything you have mentioned although not 7 days a week, more like 4![]()
I'm going to add the RYR because nothing has helped much so far.
OK, Fine Ill go back to the beginning and check the 1st post and do the math. lol
Looks like just about 1yr using the RYR?
kelkel, quick question. Is the ryr more or less effective taken with or without food?
One year. Omg. I really dislike the taste of this stuff. I drink it with the water and don't throw into a shake because ruins the taste of the shake!
Been mixing ryr with orange juice. Seems to go down easier for me that way.
I've been following a pretty hard core keto diet for the last 4 months. About 80 percent fat, the rest protein & trace carbs. Absolutely no sugars of any sort. Getting blood work done later this week & very interested to see how it effects the LDL particle size (my primary reason for doing it). The popular theory seems to be that it is the blood glucose that is causing LDL to oxidize & become small particle. I should have something to report soon.
As a little teaser, I have previously reduced my Small LDL-P from 914 (which put me in the high risk range), down to where I got it to before starting my keto experiment which was 350 (normal range but I'd still like to se it lower). I did this by lowering my carb intake & adding in a couple TBSP's of coconut oil per day. That is a pretty drastic improvement & that is also what encouraged me to just say **** it & go full keto to see what kind of results I can get from that.
Yes I have. Fibrinogen also. I don't have the #'s in front of me but CRP has always stayed in check. I have used a tsp of fish oil/ day along with one Bayer aspirin for the last few years now. I've read research suggesting that both of these have a positive influence on CRP.
Other supps that I use for heart health are 1500 mg's niacin/ day (This made a drastic improvement in my HDL), lecithin granules & also CoQ10.
Back to the CRP subject, CRP being an inflammatory marker I would expect it to come down even more on a keto diet. I believe carbohydrates to be highly inflammatory, & another carbohydrate theory that I have recently read is that it is that same carbohydrate induced inflammation in the endothelial cell lining of the arteries that actually allows plaque to accumulate. With no inflammation, the large buoyant LDL particles would pass through harmlessly.
Agreed. I wrote this a while back and will post it here. It may or may not have been said already.
Edit: Also want to add that some postulate that over consumption of Omega 6 fatty acids can lead to atherosclerosis as well.There are several theories postulated to explain the underlying cause of atherosclerosis and the mechanisms of atherogenesis remain uncertain. The response-to-injury hypothesis is the most widely accepted proposal which proposes that vascular injury starts the atherosclerotic process. Normal arteries have a smooth lining and when this lining becomes irritated a cascade of events begins that results in atherosclerosis. The body’s immune system responds by producing inflammation within the artery, triggering certain cells to deposit cholesterol and other substances under the artery’s lining, resulting in the development of lesions. The earliest pathologic lesion of atherosclerosis is known as a fatty streak. The fatty streak is the result of the accumulation of serum lipoproteins within the intima of the vessel wall. Once inside the vessel wall, LDL particles can become more prone to oxidation. Endothelial cells respond by attracting monocyte white blood cells, causing them to leave the blood stream, penetrate into the arterial walls and transform into macrophages. The macrophages' ingestion of oxidized LDL particles triggers a cascade of immune responses which over time can produce an atheroma (plaque) if HDL removal of fats from the macrophages does not keep up. Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ. Developing atherosclerotic plaques acquire their own microvascular network, the vasa vasorum, which are prone to hemorrhage and contribute to progression of atherosclerosis. If this plaque ruptures resulting in a thrombus formation, a partial or complete occlusion of the blood vessel may occur presenting with acute symptoms and possibly a heart attack or stroke.
Last edited by Who_Am_I; 05-31-2015 at 10:03 PM.
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Last edited by Pale1; 06-01-2015 at 06:45 AM. Reason: Double post
YES! Omega 6's are inflammatory while Omega 3's are anti-inflammatory, & it's all about getting the right balance between the two. Before modern man started making all those nasty vegetable oils, about the most wide spread ratio of the two fats that he may consume would be like a 4-1 Omega 6 to Omega 3. Many cultures like the Inuites consumed a 1-1 ratio. A person consuming the standard American diet is consuming a ratio of something like 16-1!!
A well structured diet should have a low Omega 3 requirement because the Omega 6 intake should already be very low (remember it's all about the ratio). Most fats should come from saturated fats (grass fed animal fats or butter), & monounsaturated fats (olive oil & avocados).
This is a book, literally:
http://www.karger.com/Article/Pdf/381654
If nothing else, read the conclusion, save it to file, etc...
Remember, it's not about the money...
The new guideline will eventually increase the numbers of
statin users on the order of millions.
Speaking of cholesterol, I watched an interesting moving the other day called The Widowmaker. It's about heart disease, stents, cholesterol and of course the corrupt medical system and doctors.
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